Pulmonary Embolism

OVERVIEW

• Pulmonary embolism (PTE, PE) ranges from asymptomatic to a life threatening catastrophe
• PE occurs when a deep vein thrombosis migrates to the pulmonary arterial tree

Types

• massive PE is defined as acute PE with obstructive shock or SBP <90 mmHg
• submassive PE is acute PE without systemic hypotension (SBP ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis
• those with none of the above severe features are non-massive or low risk PEs

PATHOPHYSIOLOGY

• effects are proportional to the rapidity and degree of obstruction
• increased PVR -> RVF -> obstructive shock
• increased alveolar dead space -> V/Q mismatch -> pulmonary vasoconstriction to optimize gas exchange
• pulmonary infarction
• chronic pulmonary hypertension can ensue

OVERALL APPROACH

CLINICAL FEATURES

History

• may be asymptomatic
• SOB
• pleuritic chest pain
• apprehension
• cough
• haemotypsis
• leg pain
• collapse = massive PE
• acute cardiovascular collapse

Examination

• pale, mottled skin
• tachypnoea
• tachycardia
• signs of DVT
• hypotension
• altered LOC
• elevated JVP
• parasternal heave
• loud P2
• central cyanosis

RISK FACTORS

Major (relative risk 5-20) – SLOMMP

• Surgery – major abdominal/pelvic, hip/knee replacements, post ICU
• Lower limb problems – #, varicose veins
• Obstetrics – late pregnancy, C/S, puerperium
• Malignancy – abdominal/pelvic, advanced/metastatic
• Mobility – hospitalization, institutional care
• Previous VTE

Minor (relative risk 2-4) – COM

• Cardiovascular – congenital heart disease, CHF, HT, superficial venous thrombosis, CVL
• Oestrogens – OCP, HRT
• Miscellaneous – COPD, neurological disability, occult malignancy, thrombotic disorder, long distance travel, obesity, other (IBD, nephrotic syndrome, dialysis, myeloproliferative disorders, paroxysmal nocturnal haemoglobinuria, Bechet’s disease)

Thrombophillias

• Factor V Leiden mutation
• Prothombin gene mutation
• Hyperhomocysteinaemia
• Antiphospholipid antibody syndrome
• Deficiency of antithrombin III, protein C or protein S
• High concentrations of factor VIII or XI
• Increased lipoprotein (a) -> test in those < 50years with recurrent or a strong FHx

INVESTIGATIONS

• goal = confirm diagnosis + assess severity
• normal compliance and peak pressures on ventilator
• increased PACO2 -> ETCO2 to gradient
• hypoxaemia

ECG:

-> mostly normal -> sinus tachycardia -> SI, QIII, TIII -> non specific ST changes or TWI in anterior leads (right heart strain), -> right axis deviation -> s wave (I and aVL) > 1.5mm -> Q wave in III and aVF -> p pulmonale -> RBBB

• CXR: rules out other pathology, focal oligaemia, wedge density (pulmonary infarction)
• ABG: reduced PaO2 in keeping with size of PE, metabolic acidosis with circulatory collapse, respiratory alkalosis
• D-Dimer: reassuring if negative to exclude PE, use in conjunction with clinical probability
• TNT: elevation is associated with adverse outcome even in normotensive patients, also associated with haemodynamic instability in patients with non-massive PE
• BNP and NT-terminal BNP: if low correlates well with uneventful course
• CTPA: as good as pulmonary angiography (gold standard), can calculate RV/LV ratio (>0.9) = severe
• ECHO: RV dialation, paradoxical septal motion towards the LV, TR, RVF, PHT or PA thrombus on TOE,
• US: leg veins (not as accurate as initially thought -> have low threshold to re-scan)

• V/Q scan: only really used now when CT is contraindicated (normal scan, low, intermediate and high probability with various criteria)
• MRI – high rate of technical difficulty and insufficient sensitivity (PIOPED III study)

MANAGEMENT

Grade severity of PE

• MASSIVE – haemodynamically unstable -> thrombolyse/embolectomy
• SUB-MASSIVE – haemodynamically stable with evidence of RV dysfunction -> strongly consider thrombolysis/embolectomy but need to balance risk of bleeding
• NON-MASSIVE – haemodynamically stable with normal RV function -> anticoagulation

Management Goals

(1) prevent further embolism (2) removal of emboli (massive or sub-massive) (3) haemodynamic support (massive)

Resuscitation

• A – may need intubation if in cardiovascular collapse or cardiac arrest
• B – high flow O2 as a pulmonary vasodilator, ventilation to optimize V/Q mismatch, hyperventilation to clear CO2
• C – invasive monitoring, fluid management to optimize right ventricular function, inotropic support, cautious fluid boluses, use milrinone, noradrenaline or adrenaline (rather than alpha agonists)

Specific Treatment

THROMBOLYSIS

• not used in non-massive or low risk PEs
• use in submassive PEs is contentious – doesn’t reduce mortality but does reduce deterioration
• can be used up to 14 days after symptoms begin
• PE resolve more quickly than with heparin alone
• as successful as embolectomy in massive PE (earlier the better)
• indicated in patients with RV compromise + haemodynamically unstable
• rTPA 1.5mg/kg is maximum dose (as good through peripheral IV or CVL)
• alteplase 100 mg (0.6mg/kg) as a continuous infusion over 2 hours
• contraindications: absolute – bleeding, recent stroke, HI, current GI bleeding, relative – PUD, surgery within 7 day, prolonged CPR
• follow straight away with heparin
• if bleeds -> FFP and anti-fibrinolytics

ANTICOAGULATION

• use UFH as first dose, in massive PE and where reversal may be required
• start immediately when there is a suspicion (prior to imaging)
• LMWH as good as heparin
• give straight after thrombolysis
• then needs warfarin (INR 2-3)

SURGICAL

• embolectomy (massive PE and unresponsive to thrombolysis or is contraindicated)
• right heart catheterisation with clot destruction
• IVC filter (high risk of further embolic or recurrent PE despite adequate anticoagulation, contraindications to anticoagulation, extensive DVT, massive PE)

OTHER THERAPIES

• ECMO – its role in PE is not established but anecdotally is very effective
• IABP – has been used with vasoactive medications
• Nitric oxide – has been used with some effect

UNDERLYING CAUSE

• prophylaxis
• modify risk factors
• diagnose thrombophillia

METABOLIC

• proportional to the degree of shock
• may have a metabolic acidosis from hyperlactataemia from circulatory compromise

References and Links

LITFL

• Burns E. ECG changes in Pulmonary Embolism ECG library
• Cadogan M. CXR eponyms in pulmonary embolism. LITFL

Journal articles

• Agnelli G, Becattini C. Acute pulmonary embolism. N Engl J Med. 2010 Jul 15;363(3):266-74.
• Jaff MR et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011 Apr 26;123(16):1788-830.